T cells develop from bone marrow (BM)-derived precursors in the thymus throughout life and decline with age. Intrathymic signals that promote T cell development and then cause the age-associated decline are derived from BM-derived hematopoietic cells, thymic epithelial cells (TECs) and other stromal components. In addition to conventional T cells the thymus also supports the generation of innate cells including Natural Killer T (NKT) cells. We have focused on conventional and non-conventional T cell development through the lens of transcription factor TCF1 that works with beta-catenin to mediate gene activation and Grg proteins to repress gene expression. Germline deletion of Tcf7 gene, encoding TCF1, impairs T cell development from the earliest stages. To understand the role of TCF1 in the development we studied global gene expression patterns in TCF1-deficient thymocytes compared with cells from wilt type (WT) mice. TCF1 and beta-catenin also regulate the development of innate cells in the thymus including NKT cells. On the other hand, beta-catenin protein accumulates in aged thymocytes and correlates with age-associated thymic involution. Accordingly, enforced expression of beta-catenin in thymocytes promotes premature thymic involution. In light of these observations we posit that insights gained from the study of TCF1 and beta-catenin will inform on T cell development and age-related decline. Chronic diseases are often manifest in older people when the immune system has become compromised. When studying the role of TCF1 in T cell function we discovered that young TCF1-deficient mice were hyper-responsive to induced experimental autoimmune encephalomyelitis (EAE). These observations suggested that TCF1 may restrain spurious T cell activation in young mice and provided an opportunity to study the balance between immune- and auto-immune response. In experiments elaborated below, we demonstrate an imbalance in gut-associated CD4 T cells and make important connections with gut-microbiota that lead to enhanced EAE in TCF1-deficient mice. We posit that during normal aging age-related impaired gut integrity may participate in the impairment of age-dependent immune dysfunction. In these studies we aim to determine mechanisms by which TCF1 and beta-catenin regulate may contribute to restrain in immune response in the young mice. We hope that the understanding obtained from these studies will inform on not only activation of immune response but the necessary restraint.